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Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer
Published on: January 12, 2020
ZNF23 induces apoptosis in human ovarian cancer cells
Chuanxin Huang1, Shenglian Yang, Ruiliang Ge
1Institute of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Abstract:
We recently reported that the level of ZNF23, a KRAB-containing zinc finger protein, is reduced in human cancers and it inhibits cell growth by inducing cell cycle arrest. Here we showed that ZNF23 also induces apoptosis in ovarian cancer cells. The protein level of ZNF23 in ovarian cancers was greatly down-regulated compared with that in the normal ovaries. Introduction of ZNF23 into ovarian cancer cells led to apoptosis as demonstrated by activation of caspase-3, nuclear condensation and formation of a sub-G1 peak. This apoptotic process was correlated with loss in mitochondrial membrane potential, cytochrome c release and caspase-9 activation. Furthermore, ZNF23 induced apoptosis partially via down-regulation of Bcl-XL. Thus, our results suggest that ZNF23 may also induce apoptosis to suppress tumor cell growth and points to the possibility that its down-regulation might facilitate ovarian cancer cell survival.
Insights
Zinc finger protein ZNF23 induces apoptosis in ovarian cancer cells by activating caspases and down-regulating Bcl-XL. Reduced ZNF23 levels in ovarian cancers may promote tumor cell survival.
Area of Science:
- Molecular Biology
- Cancer Research
- Cell Biology
Background:
- Zinc finger protein ZNF23 levels are reduced in human cancers.
- ZNF23 inhibits cancer cell growth by inducing cell cycle arrest.
Purpose of the Study:
- To investigate the role of ZNF23 in inducing apoptosis in ovarian cancer cells.
- To explore the molecular mechanisms by which ZNF23 induces apoptosis.
Main Methods:
- Assessing ZNF23 protein levels in ovarian cancers versus normal ovaries.
- Introducing ZNF23 into ovarian cancer cells to observe apoptotic effects.
- Measuring caspase-3 activation, nuclear condensation, and sub-G1 DNA content.
- Evaluating mitochondrial membrane potential, cytochrome c release, and caspase-9 activation.
- Analyzing the effect of ZNF23 on Bcl-XL expression.
Main Results:
- ZNF23 protein levels are significantly down-regulated in ovarian cancers.
- ZNF23 introduction into ovarian cancer cells triggers apoptosis, evidenced by caspase-3 activation, nuclear condensation, and sub-G1 peak.
- Apoptosis induced by ZNF23 involves loss of mitochondrial membrane potential, cytochrome c release, and caspase-9 activation.
- ZNF23 partially induces apoptosis through the down-regulation of Bcl-XL.
Conclusions:
- ZNF23 induces apoptosis in ovarian cancer cells, suggesting a role in tumor suppression.
- Down-regulation of ZNF23 may contribute to ovarian cancer cell survival.
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